High-risk prostate cancer and bone mineral content loss
Men with prostate cancer lose significantly less bone mineral content (BMC) as they age than men who are free of the disease, as per research in the recent issue of BJUI The findings are important because loss of BMC can play a key role in the development of fragile bones, fractures and osteoporosis.
American scientists studied 519 participants who joined the Baltimore Longitudinal Study at an average age of 56 between 1973 and 1984. The maximum follow-up was 35 years and the median was 22 years. Seventy-six men who participated in the study were later diagnosed with prostate cancer, with just under a quarter (24 per cent) falling into the high-risk category.
When they charted the individual BMCs of the study subjects over an extended period, the scientists could clearly see that the decline was much larger in healthy men than in men later diagnosed with prostate cancer, particularly those with high-risk prostate cancer. This occurred despite the fact that the initial baseline readings were very similar for all three groups.
The scientists also adjusted the figures to take account of other factors that affect BMC, such as smoking status, body mass index, dietary calcium and vitamin D. However, this did not change the significant differences between the healthy men and those with prostate cancer.........
In its early stages, prostate cancer requires androgens (hormones that promote the development and maintenance of male sex characteristics) for growth, and current first-line therapies target the receptor for these hormones to slow cancer's development and spread.
However, advanced prostate cancers are often androgen-independent, meaning that androgen-blocking therapies are ineffective.
Researchers aren't sure how this shift occurs as prostate cancer advances. One idea is that prostate cancer cells acquire the ability to make their own androgen. Another says that the androgen receptor that is known to stimulate tumor growth can still be active even when the hormone is not present. Most likely, both are important.
A recent study by UNC researchers, reported in the Journal of Biological Chemistry, provides evidence for the second theory, demonstrating that expression of one of a group of genes found only in humans and non-human primates can promote androgen receptor activity in concert with other proteins called coregulators.
One of a group of MAGE genes, so named because they were originally identified in melanoma, called MAGE-11 interacts with another protein, called p300, to provide the cancer cells with a way to enhance androgen receptor signaling and promote tumor growth, even when patients are undergoing androgen deprivation treatment.........
Radical cuts to social welfare spending to reduce budget deficits could cause not just economic pain but cost lives, warn experts as per a research findings published on bmj.com today.
While there is a major debate under way about the potential economic impacts of radical budget cuts in Europe, David Stuckler from the University of Oxford and colleagues dissect the effect of public spending on people's health.
Their analysis shows that levels of social spending in Europe are "strongly associated" with risks of death, particularly from diseases relating to social circumstances, such as heart attacks and alcohol-induced illness.
As such, they argue that, eventhough governments may feel they are protecting health by safeguarding healthcare budgets, social welfare spending is as important, if not moreso, for population health.
The team reviewed data on social welfare spending collected by the Organisation for Economic Cooperation and Development (OECD) from 15 European countries in the years 1980 to 2005. This includes programmes to provide support to families and children, help the unemployed obtain jobs, and support for people with disabilities, all of which could plausibly affect health.
They analysed the relationship between trends in these data and social spending. They observed that when social spending was high, mortality rates fell, but when they were low, mortality rates rose substantially.........
Colorectal cancer, cancer of the colon and rectum, is a common cause of mortality worldwide. Statistical data showed that the number of deaths caused by colorectal cancer is increasing in both men and women. Proteins are functional components of the cell that regulate the cell's activity. Understanding the differential expression of proteins in colorectal cancer and normal tissues will lead to a better understanding of the development of the disease, furthermore, these proteins may serve as biomarkers for therapy or detection of the disease. Hydrophobic proteins play a vital role in various cellular processes, by virtue of their cellular location, and may serve as a target for drug-targeted treatment.
This study, led by Assoc. Prof. Dr. Gam Lay Harn from Universiti Sains Malaysia, Malaysia will be published on June 14, 2010 in the World Journal of Gastroenterology By using two-dimensional gel electrophoresis (2D-PAGE), the hydrophobic proteins extracted from colorectal cancer tissues were separated as per their pI and MW, subsequently the protein profiles between malignant and normal tissues were compared. Using this approach, the scientists identified a few differentially expressed proteins that were up-regulated in malignant tissues. The expression of such proteins was shown to be significantly correlation to stage and grade of the cancer and also to gender of the patients.........
Stephanie Fraley, a doctoral student in chemical and biomolecular engineering, was lead author of the study. Photo by Will Kirk/HomewoodPhoto.jhu.edu
Showing movies in 3-D has produced a box-office bonanza in recent months. Could viewing cell behavior in three dimensions lead to important advances in cancer research? A newly released study led by Johns Hopkins University engineers indicates it may happen. Looking at cells in 3-D, the team members concluded, yields more accurate information that could help develop drugs to prevent cancer's spread.
The study, a collaboration with scientists at Washington University in St. Louis, appears in the recent issue of Nature Cell Biology.
"Finding out how cells move and stick to surfaces is critical to our understanding of cancer and other diseases. But most of what we know about these behaviors has been learned in the 2-D environment of Petri dishes," said Denis Wirtz, director of the Johns Hopkins Engineering in Oncology Center and principal investigator of the study. "Our study demonstrates for the first time that the way cells move inside a three-dimensional environment, such as the human body, is fundamentally different from the behavior we've seen in conventional flat lab dishes. It's both qualitatively and quantitatively different".
One implication of this discovery is that the results produced by a common high-speed method of screening drugs to prevent cell migration on flat substrates are, at best, misleading, said Wirtz, who also is the Theophilus H. Smoot Professor of Chemical and Biomolecular Engineering at Johns Hopkins. This is important because cell movement is correlation to the spread of cancer, Wirtz said. "Our study identified possible targets to dramatically slow down cell invasion in a three-dimensional matrix".........
Virginia Commonwealth University scientists have discovered a mechanism by which an enzyme regulates gene expression and growth in melanoma cells, a finding that could someday lead to more effective drugs to attack cancers and make them more treatable.
Melanoma, the most serious type of skin cancer, is highly resistant to current therapeutic strategies for reasons that are not well understood. New research at VCU suggests that an enzyme discovered in 2003 might be used to target a specific genetic component that helps to regulate gene expression and defends melanoma cells against therapy.
The findings are reported online this week in the Proceedings of the National Academy of Sciences.
"By selectively and specifically targeting molecules for degradation that serve as gatekeepers for cancer growth, progression and resistance to treatment, it appears to be possible to turn the cancer cells' defense into an offense that can be used as an effective approach to destroy the tumor," said Paul B. Fisher, Ph.D., professor and chair of the Department of Human and Molecular Genetics and director of the VCU Institute of Molecular Medicine in the VCU School of Medicine.
Several years ago, Fisher led a team of researchers at Columbia University in identifying an enzyme involved in halting the growth of human cancerous melanoma and other cancer cells. The enzyme, called human polynucleotide phosphorylase or hPNPaseold-35, drives malignant cells to irreversibly lose their growth potential and acquire properties of more normal cells, a process called terminal cell differentiation. The enzyme also is important in cellular senescence, when a cell cannot divide anymore and dies. Additionally, the researchers developed new strategies for promoting cancer cell-specific expression of this enzyme, which reduced tumor growth in animal cancer models.........
The combination of two different chemotherapies and a previously approved therapy for kidney and liver cancers is not effective against advanced melanoma, as per results disclosed in an oral presentation today at the 46th annual meeting of the American Society of Clinical Oncology (ASCO) in Chicago.
"With each newly released study, we learn something important about the therapy of melanoma," said John M. Kirkwood, M.D., professor of medicine, University of Pittsburgh School of Medicine, and leader of the University of Pittsburgh Cancer Institute's (UPCI) melanoma and skin cancer program. "With this study, we learned that the addition of sorafenib, a molecular inhibitor, to a traditional chemotherapy regimen does not improve patient survival".
The phase III trial, which was sponsored by the Eastern Cooperative Oncology Group (ECOG), enrolled 823 patients from seven different sites across the country over 34 months. The primary goal of the study was to determine whether the addition of sorafenib, a molecular targeting agent, would improve survival rates for patients with metastatic melanoma when added to the chemotherapy combination of carboplatin and paclitaxel. Patients either received the chemotherapy combination alone or with sorafenib.
"While this study didn't confirm the very promising results of phase II studies with sorafenib, it is important to share its findings since the double chemotherapy combination of carboplatin and paclitaxel has achieved results that eclipse prior chemotherapy results in large phase III trials. These results take us one step closer to understanding how to most effectively treat metastatic melanoma," said Dr. Kirkwood.........
Breast and patients with prostate cancer who regularly exercise during and after cancer therapy report having a better quality of life and being less fatigued, as per scientists at Henry Ford Hospital in Detroit.
"Using exercise as an approach to cancer care has the potential to benefit patients both physically and psychologically, as well as mitigate therapy side effects," says study main author Eleanor M. Walker, M.D., division director of breast services in the Department of Radiation Oncology at Henry Ford Hospital.
"Plus, exercise is a great alternative to patients combating fatigue and nausea who are considering using supplements which may interfere with medications and chemotherapy they're taking during cancer therapy."
Dr. Walker will present a poster with the study's design and intervention methods June 7 at the 2010 American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago. The abstract is now available online at www.ASCO.org.
To study how exercise impacts cancer patients, Dr. Walker and her colleagues at Henry Ford's Josephine Ford Cancer Center and the Henry Ford Heart & Vascular Institute developed a unique program called ExCITE (Exercise and Cancer Integrative Therapies and Education).
ExCITE works with patients who are receiving cancer therapy to create individualized exercise programs. Some patients come into one of Henry Ford's fitness centers to workout, while others have plans that allow them to exercise at home during various stages of their care.........
Mice bearing the mutation that causes familial adenomatous polyposis in human beings (Min mice) develop small intestinal tumors that express COX-2. Fluorocoxib injection into Min mice lights up an intestinal polyp.
Credit: Lawrence Marnett, Ph.D., and colleagues
A series of novel imaging agents could light up tumors as they begin to form before they turn deadly and signal their transition to aggressive cancers.
The compounds fluorescent inhibitors of the enzyme cyclooxygenase-2 (COX-2) could have broad applications for detecting tumors earlier, monitoring a tumor's transition from pre-malignancy to more aggressive growth, and defining tumor margins during surgical removal.
"We're very excited about these new agents and are moving forward to develop them for human clinical trials," said Lawrence Marnett, Ph.D., the leader of the Vanderbilt University team that developed the compounds, which are described in the May 1 issue of Cancer Research.
COX-2 is an attractive target for molecular imaging. It's not found in most normal tissues, and then it is "turned on" in inflammatory lesions and tumors, Marnett explained.
"COX-2 is expressed at the earliest stages of pre-malignancy in pre-cancerous lesions, but not in surrounding normal tissue and as a tumor grows and becomes increasingly cancerous, COX-2 levels go up," Marnett said.
Compounds that bind selectively to COX-2 and carry a fluorescent marker should act as "beacons" for tumor cells and for inflammation.
Marnett and colleagues previously demonstrated that fluorescent COX-2 inhibitors which they have now dubbed "fluorocoxibs" were useful probes for protein binding, but their early molecules were not appropriate for cellular or in vivo imaging.........
It is an accepted fact that genetics play a key role in a person's susceptibility to cancer, and that throughout life, mutations can cause damage to tumor suppressor genes (TSGs) further increasing the chances of developing malignant tumors.
Now a newly released study led by researchers at Beth Israel Deaconess Medical Center (BIDMC) demonstrates that even subtle changes in expression of the PTEN tumor suppressor gene can significantly increase cancer susceptibility in specific tissues, suggesting that environmental factors, such as diet or exposure to carcinogens, may have a more dramatic influence on tumor development than previously recognized. Appearing in this week's Advance On-line issue of Nature Genetics, the findings propose a new model for the role of tumor suppressor genes in the onset of cancer and could prove valuable in the development of diagnostic tests targeted to these gene alterations.
"More than 30 years ago, it was proposed that a person's susceptibility to cancer was dependent on a 'two-hit' model," explains Pier Paolo Pandolfi, MD, PhD, Director of the Cancer Genetics Program at BIDMC and George C. Reisman Professor of Medicine at Harvard Medical School. This meant that there had to be two genetic alterations of a single tumor suppressor gene (TSG) to activate tumor development one gene would be missing from birth, while the second would be lost to other factors during one's lifetime.........
Jay Groves (foreground) and Pradeep Nair used TIRF imaging and their own spatial mutation strategy to discover a new way in which cells can sense and respond to physical forces. (Photo by Roy Kaltschmidt, Berkeley Lab Public Affairs)
Conventional biological wisdom holds that living cells interact with their environment through an elaborate network of chemical signals. As a result a number of therapies for the therapy of cancer and other diseases in which cell behavior goes awry focus on drugs that block or disrupt harmful chemical signals. Now, a new road for future therapies may have been opened with scientific evidence for a never seen before way in which cells can also sense and respond to physical forces.
A team of scientists with the Lawrence Berkeley National Laboratory (Berkeley Lab) and the University of California (UC) Berkeley has shown that the biochemical activity of a cellular protein system, which plays a key role in cancer metastasis, can be altered by the application of a direct physical force. This discovery sheds important new light on how the protein signaling complex known as EphA2/ephrin-A1 contributes to the initiation, growth and progression of malignant cells, and also suggests how the activity of cancer cells can be affected by surrounding tissue.........
Cancer in the other breast in women with breast cancer
Postmenopausal women, including those over 70 years old, who have been newly diagnosed with cancer in one breast have higher cancer detection rates when the other breast is scanned for tumors with MRI, in comparison to premenopausal women, say scientists at the Mayo Clinic campus in Florida.
They observed that 3.8 percent of 425 women had breast cancer in the undiagnosed breast that had not been found with a clinical or mammographic examination; all were postmenopausal. In these women, detecting and treating cancer in both breasts at the same time may save costs, patient stress, and the potential toxicity that may come from having to treat cancer later in the second breast once it is discovered, the scientists say in the March/recent issue of The Breast Journal.
Of particular interest to the scientists is their finding that patients 70 and older had a higher prevalence of cancer detected in the second breast by MRI than did younger patients in the study. MRI detected a cancer in the second breast in 5.4 percent of 129 elderly women included in the study.
"Our findings are not really surprising because we know that the risk of breast cancer increases as age increases," says the study's lead investigator, Johnny Ray Bernard Jr., M.D., a Radiation Oncologist at Mayo Clinic in Jacksonville. "Elderly women in good health potentially benefit from earlier detection, and we think that screening of the undiagnosed breast with MRI should be considered in all postmenopausal women diagnosed with a breast cancer."........
A mutation in a single gene can cause endometrial cancer that is responsive to a specific drug treatment, scientists at UT Southwestern Medical Center have found in an animal study.
The finding suggests that eventually it might be possible to screen women with endometrial cancer to see if they have that mutation and use the drug as targeted treatment, the scientists said.
"Our data suggest that deficiency of this gene can indicate both how aggressive an endometrial tumor will be and how well it might respond to a specific class of drugs," said Dr. Diego Castrillon, assistant professor of pathology at UT Southwestern and senior author of the paper, which appears in the March/recent issue of Disease Models and Mechanisms
"Some early clinical trials have shown that about one-fifth of women with endometrial cancers respond to a group of drugs called 'rapalogs,'" Dr. Castrillon said. "Unfortunately, it is not currently possible to predict which women these are".
Endometrial cancer affects the lining of the uterus. This cancer is the most common cancer of the female reproductive tract and is commonly detected when a woman complains of excessive bleeding. About one-third of ovary cancer cases are believed to begin as endometrial cancer, Dr. Castrillon said. The median survival of women with advanced endometrial cancer is one year.........
Endometrial cancer is the most common cancer of the female reproductive tract, representing 6% of all cancers. There is currently no screening method or biomarker to indicate early presence of disease. "It is a very common malignancy that affects women of all ages" comments paper author Dr. Diego Castrillon. The cancer forms from the cells that grow along the inner lining of the uterus, which is called the endometrium, and commonly it is diagnosed following patient reports of abnormal bleeding.
The normal endometrium is a dynamic place, providing a thick, highly vascularized environment ready to generate a placenta if it is implanted with an embryo. The dynamic and cyclic activity of the endometrium makes it very sensitive to signaling molecules. Early changes in many signaling proteins are known to contribute to endometrial cancer in some patients. A major research goal is to understand how signals create cancer cells and to identify places where intervention might shut down the signals that promote cancer cell survival and growth.
Scientists learn about cancer by creating genetic changes to signaling proteins in mice that reflect changes found in human cancer patients. Animal models are produced in this way to help understand how cancer cells form and progress. One challenge is to localize genetic changes to the environment of interest. In the case of endometrial cancer, scientists need to specifically modify only those cells that are in the endometrium, so that their data is not complicated by changes in other tissues.........
Sociologists at Case Western Reserve University observed that when passive cancer patients become survivors, they have plenty of bold advice to offer other cancer patients, as per a research studyin JAGS, the Journal of American Geriatric Society
Eva Kahana, Robson Professor of Sociology and director of the Elderly Care Research Center at Case Western Reserve, reported the findings from interviews with 100 cancer survivors. These survivors are part of a longitudinal study of 1,107 older adults living in a retirement community.
This study calls attention to generally accepting, timid behaviors that elderly patients report about their interactions with the healthcare system while battling cancer. Nevertheless the very same elderly adults offer advice to other older cancer patients to take a more activist stand and become advocates in their care.
This finding of the study overturns the notion that elderly patients are disinterested and disempowered health consumers, Kahana said.
For nearly 20 years, the longitudinal study's research team gathered information from this Florida retirement community to find out what older people do to age successfully and weather chronic illnesses and the frailties in their later years.
In the study's 17th year, cancer survivors were given an in-depth interview with open- and close-ended questions about their cancer experience. The participants were of an average age of 79, married (62%) and were mostly women (62%). The predominant cancers were breast and prostate.........
Dr. Mamdooh Ghoneum is a researcher at Charles Drew University.
Credit: Charles Drew University
A researcher at Charles Drew University of Medicine and Science is investigating the potential use of non-pathogenic baker's yeast as a promising, natural treatment for cancer.
Dr. Mamdooh Ghoneum presented his findings Tuesday, Feb. 2 at a special conference on "Cell Death Mechanism," sponsored by the American Association for Cancer Research (AACR) at the Omni San Diego Hotel in San Diego.
"The central focus of the meeting is cell death regulation and how to mine and exploit it for therapeutic gain," a written assessment of the AACR special conference states. "This conference includes new complexities of cell death and cell survival, new technologies, and clinical translational aspects necessary for the evolution of new therapeutic strategies".
For more than two decades, Dr. Ghoneum has pursued a theory that cancer cells self destruct when exposed to small quantities of yeast.
In laboratory tests, Dr. Ghoneum exposed cancer cells to yeast and observed as they ingested the yeastthrough a process known as phagocytosisand then the cancer cells died. First, he investigated this phenomenon in test tubes (in vitro), introducing yeast to breast, tongue, colon, and skin cancers.
"I have no doubt that I am close to unlocking the mystery as to why cancer cells weaken to the point of destruction after eating common baker's yeast," Dr. Ghoneum said. "The cells just gravitate to the yeast. I call it fatal attraction".........
Taxanes, a group of cancer drugs that includes paclitaxel (Taxol) and docetaxel (Taxotere), have become front-line treatment for a variety of metastatic cancers. But as with a number of chemotherapy agents, resistance can develop, a frequent problem in breast, ovarian, prostate and other cancers. Now, cancer scientists at Children's Hospital Boston report a protein previously unknown to be involved in taxane resistance and that could potentially be targeted with drugs, making a cancer more susceptible to chemotherapy.
The scientists think that this protein, prohibitin1, could also serve as a biomarker, allowing doctors to predict a patient's response to chemotherapy with a simple blood test. The study was published online by the Proceedings of the National Academy of Sciences in its online early edition during the week of January 25.
The study, led by Bruce Zetter, PhD, of Children's Vascular Biology Program, used proteomics techniques to compare the proteins present in Taxol-susceptible versus Taxol-resistant human tumor cell lines. The scientists observed that the resistant cell lines, but not the susceptible cell lines, had prohibitin1 on their surface. When they suppressed prohibitin1 with RNA interference techniques, the tumor cells became more susceptible to Taxol, both in cell culture and in live mice with implanted Taxol-resistant tumors.........
New Rochelle, NY, January 15, 2010Opinion leaders in the field of palliative medicine explored the unparalleled opportunities that now exist for the palliative care community, which matches therapy to the desires of informed patients and their families, to help define evolving health care reform policy. The thought-provoking Roundtable discussion, "Palliative Medicine: Politics and Policy," is published online ahead of print in Journal of Palliative Medicine, a peer-evaluated publication from Mary Ann Liebert, Inc. (www.liebertpub.com). The Roundtable is available free online at www.liebertpub.com/jpm.
The moderator, Diane E. Meier, MD, from the Center to Advance Palliative Care at Mount Sinai School of Medicine, in New York City, led a lively discussion focusing on the need to change public perception of palliative care and to educate the public and policymakers on how palliative medicine can contribute to improved quality and greater cost-effectiveness of health care, two of the cornerstones of current health care reform efforts. In October 2009, Dr. Meier began a health policy fellowship in Washington, D.C., with the goal of learning how process and politics influence health policy.
Participants in the Roundtable included David J. Casarett, MD, from the Philadelphia Veterans Administration Medical Center and the University of Pennsylvania, Charles F. von Gunten, MD, PhD, Editor-in-Chief of Journal of Palliative Medicine, and Provost, Institute for Palliative Medicine at San Diego Hospice (California), Walter J. Smith, SJ, PhD, from HealthCare Chaplaincy (New York City), and C. Porter Storey Jr., MD, from the American Academy of Hospice and Palliative Medicine (Glenview, IL) and Colorado Permanente Medical Group (Denver).........
How often patients receive surveillance colonoscopy may need to be better aligned with their risks for colorectal cancer, as per two papers published this month by University of Pittsburgh School of Medicine researchers. The studies provide evidence that colonoscopy is both overused and underused in particular patient populations with serious implications for health care spending.
As per Robert E. Schoen, M.D., M.P.H., professor of medicine and epidemiology at the University of Pittsburgh and senior author of both papers, surveillance colonoscopy is performed to monitor patients who have had premalignant polyps, called adenomas, found on a prior colonoscopy. The aim of surveillance is to identify and remove recurrent growths before they advance to cancer.
"Guidelines recommend that patients who have had pre-malignant lesions, particularly advanced premalignant lesions, get follow-up colonoscopy earlier and more often than patients who do not have polyps," said Dr. Schoen. "Yet our studies show surveillance colonoscopy is not being used by the medical system in relation to underlying risk".
The first study, reported in the January edition of the journal Gastroenterology, demonstrates a substantial overuse of surveillance colonoscopy among low-risk patients and under-use among high risk patients. The study followed 3,600 patients from the National Cancer Institute (NCI)-sponsored Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial. Among 1,026 patients with no premalignant lesions at their initial examination, 58 percent underwent a follow-up exam an average of every 3.9 years, eventhough the recommendation would be to do so every five or 10 years. Detailed review of the records could not identify medical reasons for the premature testing. After five years, only 58.4 percent of patients with advanced premalignant lesions received surveillance colonoscopy despite the recommendation that they do so every three years.........
Researchers in China are reporting discovery of two proteins present in the blood, of people with colon cancer that may serve as the potential biomarkers for accurately predicting whether the disease will spread. Their study is in ACS' Journal of Proteome Research, a monthly publication.
Maode Lai and his colleagues note that in 2008, 150,000 new cases of colon cancer and over 50,000 deaths from the disease occurred in the United States alone. Surgery is the main method of treating the disease. However, half of patients with colon cancer undergoing surgery develop a recurrence of the disease within 5 years due to its spread, or metastasis, to other parts of the body. The spread of colon cancer can be difficult to detect and there are currently no reliable chemical markers in the body for predicting its spread, the researchers say.
In an effort to identify useful biomarkers for tracking the spread of colon cancer, the researchers compared proteins produced by primary, or original, tumor cells to those of metastasized cells came from a single individual with colon cancer. They identified two proteins that occurred at significantly higher levels in the metastatic cells than in the primary cancer cells. The two proteins could serve as potential biomarkers in a blood test for predicting the spread of colon cancer, allowing earlier intervention and therapy, the researchers say.........
Cancer of the gullet, or oesophagus, is one of the ten most common cancers in the Western world, and there have been recent alarming increases in the number of cases each year in the US and UK. There is no good therapy, and sufferers frequently face a short, painful battle which ends all too quickly in death. A number of of the cancers diagnosed are in people with a long history of heartburn. Chronic heartburn leads to the lower parts of the gullet being bathed in a toxic acid solution, and the lining of the gullet defends itself against this by changing itself into something which looks a lot like the lining of the lower intestines. Eventhough the damaged tissue, called Barrett's oesophagus, is not malignant in itself, its presence warns doctors that the patient has taken the first step towards cancer, and triggers a rigorous programme of monitoring, coupled with treatment to prevent further damage.
Patients with Barrett's oesophagus can be stabilised, and most do not go on to develop cancer, but once it is there, the mutated tissue is almost impossible to eradicate, so the risk always remains. Scientists have long been searching for new drugs able to revert Barrett's oesophagus to the healthy, normal lining of the gullet, and now, a team led by Hans Clevers of the Hubrecht Institute, Utrecht, may have a candidate. Clevers' team, whose research into colon cancer is world-renowned, reasoned that as Barrett's oesophagus cells are very similar to the cells which line the colon, they might share vital control pathways. This turns out to be true. Clevers and his team then put this together with the fact that the anti-Alzheimer's drug DBZ, currently in clinical trials, is known to have side effects on the lower gut lining. They used a rat model of oesophageal cancer to observe the effects of DBZ on Barrett's oesophagus tissue, and observed that DBZ could halt the growth of Barrett's oesophagus, and in some cases completely destroyed the mutant tissue. Whilst the therapy is still a long way from being trialled in humans, it is an exciting step forward in the fight for a cure for oesophageal cancer.........
Charles M. Rudin, M.D., Ph.D. is the associate director for clinical research at the Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins.
Credit: Charles M. Rudin, M.D., Ph.D.
People with the heritable disorder of the skin called Gorlin syndrome who are genetically predisposed to develop basal cell carcinoma of the skin may have a new chemoprevention treatment on the horizon.
As per results of a placebo-controlled, randomized, double-blind, Phase II study, the use of celecoxib was effective in inhibiting the development of basal cell carcinomas in a relatively rare group of patients who are highly susceptible to carcinoma. These findings appear in the recent issue of Cancer Prevention Research, a journal of the American Association for Cancer Research.
Celecoxib, sold under the brand name of Celebrex by Pfizer Inc., is a non-steroidal anti-inflammatory drug (NSAID). Patients with Gorlin syndrome typically develop hundreds or even thousands of basal cell carcinomas in their lifetime.
Ervin H. Epstein Jr., M.D., senior scientist at the Children's Hospital of Oakland Research Institute, Oakland, Calif., said the goal of this study was to reduce the number of basal cell carcinomas in patients with this rare disorder who are most at risk for this form of cancer.
"The underlying idea is if we can find something in these high-risk patients that could be translatable to the 'normal' population, then we could ultimately use that form of chemoprevention to reduce the numbers of skin cancer in all people," he said.........
Current research suggests that TNF-receptor associated protein-1 (TRAP-1) may prevent cancer cell death. The related report by Leav et al, "Cytoprotective Mitochondrial Chaperone TRAP-1 as a Novel Molecular Target in Localized and Metastatic Prostate Cancer," appears in the January 2010 issue of the American Journal of Pathology
Prostate cancer is the most common type of cancer and is the second leading cause of cancer deaths among men in the United States, following lung cancer. Prostate cancer most usually develops in men over the age of 50 and is slow-growing; however, it may metastasize to other organs, particular to the bones and lymph nodes. Metastatic phase prostate cancer claims over 30,000 deaths per year in the United States alone.
Prostate cancer cells are often resistant to cell death. Scientists led by Dr. Dario C. Altieri of the University of Massachusetts Medical School, therefore, explored the role of TRAP-1, a protein thought to regulate cell death, in prostate cancer survival. TRAP-1 was highly expressed in both high-grade human prostate cancer lesions and mouse models of prostate cancer, but not in non-malignant or normal prostate tissue. In addition, TRAP-1 overexpression in non-cancer prostate cells inhibited cell death, whereas TRAP-1-deficient prostate cancer cells had enhanced levels of cell death. Moreover, therapy with Gamitrinib, which inhibits TRAP-1, resulted in prostate cancer cell death, but not death of non-malignant prostate cells. Therefore, targeting TRAP-1 via Gamitrinib therapy appears to be a viable therapeutic strategy for patients with advanced prostate cancer.........
Dr Ruth Kluck has been investigating the role in apoptosis of two proteins, Bak and Bax.
Walter and Eliza Hall Institute researchers have identified a key step in the biological process of programmed cell death, also called apoptosis.
Apoptosis is important in human biology as it removes unwanted and sometimes dangerous cells from our bodies, protecting us against cancer development. It can also, however, lead to the development of degenerative diseases when healthy cells are errantly destroyed.
The research, led by Dr Ruth Kluck from the institute's Molecular Genetics of Cancer Division, is crucial to the development of drugs that can turn on apoptosis, thereby more effectively killing cancer cells. It could also be used in developing compounds that turn off the apoptosis that leads to degenerative disorders.
Dr Kluck has been investigating the role in apoptosis of two proteins, Bak and Bax. It is thought that understanding their role will identify targets against which drugs to regulate cell death could be designed.
"The pivotal step towards cell death is the formation of a pore in the mitochondria; mitochondria make and supply energy to the cells," Dr Kluck said. "Pore formation is the point of no return in apoptotic cell death as it allows cytochrome c, which is the protein that initiates cell death, to escape from the mitochondria. Only two proteins are known to form the pore, Bak and Bax".........
A New York Medical College doctor who specializes in restoring or preserving fertility in female cancer patients has discovered a possible link between the presence of breast cancer genes and infertility.
In a paper published last week in the Journal of Clinical Oncology, Kutluk Oktay, M.D., professor of obstetrics and gynecology and principal investigator on the study, concluded that mutations in the BRCA1 gene, which have been linked with early onset breast cancer, are also linked to an early loss of egg reserves. This finding may help to explain why women who carry a mutated BRCA1 gene have greater rates of infertility as well as a greater risk for breast and ovary cancer.
Dr. Oktay's team performed ovarian stimulation in 126 women with breast cancer for the purpose of fertility preservation by embryo or oocyte cryopreservation. The results showed that of the 82 women who met the inclusion criteria, 47 women (57 percent) had undergone BRCA testing, with 14 having a mutation in BRCA genes. In BRCA mutation-positive patients, the low ovarian response rate was significantly greater than for patients who did not show BRCA gene mutations, nor for women who had not been tested for the gene at all.
If fertility drugs are not as effective in stimulating egg production in the ovaries of patients who carry BRCA1 mutations, this establishes a link between infertility and the risk of getting breast or ovary cancer, Dr. Oktay concludes.........
Heart drugs show promise for fighting colon cancer
The leaves of the oriental foxglove plant contain digitoxin, a drug used to treat heart disease. It is in a family of medications that now show promise for fighting colon cancer.
Researchers in Sweden are reporting for the first time that a group of drugs used to treat heart failure shows promise for fighting colon cancer. The study is in ACS' Journal of Natural Products, a monthly publication. Colon cancer is the third most common cancer in the United States, with more than 150,000 cases diagnosed in the U.S. each year.
Jenny Felth, Joachim Gullbo, and his colleagues note that cardiac glycosides are a family of naturally-derived drugs used to treat congestive heart failure and abnormal heart rhythms. Researchers have suspected for some time, based on prior research, that these heart drugs may have promise for fighting a number of different types of cancer. Despite this, knowledge on effects in colon cancer or combination effects with other anti-cancer drugs is lacking. But researchers know little about their potential anticancer effects and have not tested these substances against colon cancer.
As part of a larger study to screen and identify natural substances with activity against colon cancer, the researchers picked several cardiac glycosides for further study. They tested five of these heart drugs against laboratory cultures of human colon cancer cells and observed that they were all effective, to varying degrees, at killing the cancer cells. The sensitivity, however, was rather low when in comparison to that of other cancer cell types reported previously. Several of the drugs also showed increased anticancer activity when combined with certain drugs used for standard chemotherapy. The findings suggest that these heart drugs may affect colon cancer outcome when used alone or in combination with conventional chemotherapy drugs, they say.........
